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Helicobacter pylori biofilm extracellular matrix and mucus glycoproteins constitute a critical microenvironment for the survival and pathogenesis of H. pylori within the human stomach. The biofilm is a complex assembly of extracellular polymeric substances (EPS), including polysaccharides, proteins, and extracellular DNA, which shields the bacteria from the harsh acidic environment and limits the penetration of antimicrobial agents (Yonezawa et al., 2015). H. pylori specifically adheres to host gastric mucus glycoproteins, primarily MUC5AC and MUC6, through bacterial adhesins such as BabA and SabA, facilitating stable colonization and immune evasion (Linden et al., 2008). This protective barrier is a major contributor to treatment failure and the development of chronic conditions like gastritis, peptic ulcers, and gastric cancer. Therapeutic interventions often target this matrix using mucolytic agents like N-acetylcysteine or bismuth-based compounds to disrupt the biofilm structure and improve the delivery of antibiotics (Karbasi et al., 2013). By degrading the EPS and reducing the viscosity of the mucus layer, these agents expose the bacteria to the host immune system and pharmacological treatments. Understanding the interplay between the bacterial matrix and host mucins is essential for developing more effective eradication therapies for antibiotic-resistant strains.
Disruption of the biofilm matrix and mucolysis to enhance antibiotic penetration and reduce bacterial colonization.
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